Osteoarthritis (OA) is a chronic, progressive joint disease characterized by degenerative changes in articular cartilage, subchondral bone sclerosis, accompanied by synovitis and chondrocyte apoptosis. With the aging of society, it has become one of the major factors endangering the mobility of middle-aged and elderly people worldwide. The pathogenesis of OA remains unclear, and current treatments can only control symptoms without effectively repairing damaged cartilage. Ferroptosis, a novel form of programmed cell death proposed and confirmed in 2012, is characterized by iron-dependent accumulation of lipid peroxides, mitochondria-specific damage, and imbalance in antioxidant defense capacity. In recent years, it has been proven to be involved in regulating the process of cartilage degradation in OA. This review mainly focuses on the key biological processes of chondrocyte ferroptosis, elaborating on the interactions between iron homeostasis disorders, oxidative stress and inflammation, as well as the research progress on chondrocyte ferroptosis induced by dysregulation of important signaling pathways in the pathological environment of OA. In summary, it systematically analyzes the relationship between ferroptosis and other forms of programmed cell death, summarizes the research progress of OA therapeutic strategies targeting chondrocyte ferroptosis, and puts forward the existing contradictions and development trends in current research, aiming to provide new clues and directions for exploring the mechanism of OA occurrence and development and clinical personalized treatment.
Zhou et al. (Fri,) studied this question.